What happens in our bodies after weight loss? It takes a lot of effort to lose weight. Recent estimates show that 52% of Americans are trying to lose weight, and an additional 29% are trying to maintain weight loss. Up to one-third of lost pounds are regained in the first year, and as few as 6% of people maintain 5% weight loss after 6 years. Why is it such a hard task, and what do successful losers do to avoid regaining lost pounds?
Overall, the obesity picture is pretty grim: As of 2011-2012, the majority (69%) of adults in the US were either obese (BMI >30%; 35%) or overweight (BMI 25-30%; 34%). 21% of adolescents were obese, 18% of children ages 6-11, and 8% of children ages 2-5. The prevalence of adult obesity in the US has been increasing steadily since 1980, when it was 15%. Obesity rates have more than doubled in children and tripled in adolescents in the last 30 years. Poor diet/physical inactivity is the 2nd highest cause of death after tobacco use, accounting for approximately 365,000 US deaths in 2000. Total health care costs related to obesity and comorbidities were estimated to be 25% to 44% greater for obese individuals than for their normal-weight counterparts. Thus, the USDA advisory committee on dietary guidelines (2010) proclaimed obesity to be this century's most serious public health threat.
Several factors seem to thwart sustained weight loss and promote recidivism: First, the body is hardwired to maintain weight through complex hormonal feedback loops. Second, hedonic urges in some individuals can be hard to resist. Not to mention that we live in a cultural environment of sedentary lifestyles with high-fat, calorie-dense foods available everywhere.
Let's back up and talk about what happens when you lose weight. Adipose tissue is made up of adipocytes that store energy as fat. An average human adult has 30 billion adipocytes, which altogether weigh about 30 lbs. When weight is gained, fat cells increase in size about 4-fold before dividing to increase the total number of fat cells. When weight is lost, fat cells shrink but the number of fat cells never decreases. People with an excess of fat cells have a harder time losing weight and keeping it off than those with just enlarged fat cells.
Leptin, ghrelin, and other hormones act together to promote energy homeostasis and keep the weight at its set point. Leptin ("the satiety hormone") is secreted by adipocytes, circulates in the blood, and crosses the blood-brain barrier (BBB) to inhibit hunger. Acting in opposition to leptin is ghrelin ("the hunger hormone"), a peptide hormone secreted when the stomach is empty. Ghrelin crosses the BBB and acts on brain receptors to regulate appetite. When the stomach is stretched after eating, ghrelin production stops. Ghrelin levels decrease when sleep is increased; they increase with age.
In obese people, leptin concentrations are high and ghrelin concentrations are low, and their normal diurnal patterns are disturbed. It's not clear if these abnormalities are a cause or consequence of obesity. Although leptin levels are elevated, there is a decreased sensitivity to them, possibly due to reduced BBB crossing. Researchers were able to induce leptin resistance by feeding rats unlimited, palatable, energy-dense foods; this effect reversed in mice when they were put back on a low-energy diet. In another rat study, chronic leptin infusions led to leptin resistance.
Conversely, weight loss triggers decreases in leptin and increases in ghrelin. These findings support the idea that these hormones work in a homeostatic fashion to keep body weight at its set point (the body weight level at which stability has been established). The set point weight regulation system is located primarily in the hypothalamus and brainstem and has been called "the metabolic brain". The set point can drift upward gradually, possibly in response to leptin resistance. The body's innate defense against weight loss seems to be much more vigorous than its defense against weight gain. Packing on excess energy stores seems fine evolutionarily (survival of the fattest), but not losing essential energy stores and possibly starving to death. Metabolic obesity, at least in rats, has some genetic component, as not all rats respond to high-fat diets the same, and the ones that do/don't overeat can be selectively bred to never/always overeat.
In addition, in some individuals, the brain's reward system ("cognitive and emotional brain") located in the corticolimbic structures can override homeostatic metabolic signals and lead to obesity. This non-homeostatic system guides food intake based on its reward value. Dopaminergic signaling disruptions are being investigated as possible mechanisms of this "hedonic obesity". Some aspects of the dopamine reward pathway are similar in obese patients and patients with addictive states, and the concept of tolerance may apply in obesity. fMRI scans in obese individuals have demonstrated an overactivation of reward-encoding brain regions and a deficiency in frontal brain inhibitory networks in response to food stimuli.
What happens after a person loses weight?
Effects on metabolism
During weight loss, fat cells shrink below their normal size, and body weight drops below the set point. Hunger increases, and food looks even more enticing. In addition, there are decreases in blood leptin concentrations, thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in blood ghrelin concentrations, parasympathetic tone, and muscle efficiency. The body's innate metabolic homeostatic mechanisms try to get body weight back up to the set point: the basal metabolic rate (BMR) and total energy expenditure (TEE) both decrease. TEE is the total amount of energy consumed by the body; it includes BMR (resting energy expenditure), nonresting energy expenditure (eg, exercise, physical labor), and the thermic effect of feeding (energy required for digestion). TEE is calculated based on weight, height, gender, age, and activity level.
Some studies have shown an even greater than predicted reduction in TEE following weight loss, implying that the weight loss itself is triggering a metabolic slow-down. Leibel and colleagues report that after subjects lost 10% of their weight in a controlled environment, TEE per unit of fat-free mass was significantly reduced (by 6±3 kcal/kg/d in never-obese subjects and by 8±5 kcal/kg/d in formerly obese subjects). Conversely, after 10% weight gain, TEE per unit of fat-free mass was significantly increased (by 9±7 kcal/kg/d in never-obese subjects and 8±4 kcal/kg/d in formerly obese subjects). A 10% weight gain led to a TEE of 500 kcal/d above predicted, and 10% and 20% weight losses led to TEEs of approximately 300 kcal/day below predicted. Because these results were similar for the 10- and 20-lb weight loss groups, adaptation was likely reached by 10% decrease. In an earlier study, the authors found that obese subjects who were maintaining weight loss burned 28% fewer kilocalories per unit of body surface area compared with baseline values and 24% fewer than did age- and sex-matched never-obese controls.
When Rosenbaum and colleagues evaluated subjects after a recent ≥10% weight loss and after 1-6 years' weight loss maintenance vs. sex- and weight-matched controls under controlled conditions, they found significantly lower TEEs in both weight loss groups compared with the no-weight loss group, and no significant difference between the 2 weight loss groups. The authors concluded that the disproportionate decreases seen in energy expenditure persist well beyond the period of weight loss.
However, these effects have not been shown consistently. For example, Wyatt et al and Weinsier et al found no significant differences in resting metabolic rate (RMR) in reduced-obese subjects compared with weight-matched controls. To address these inconsistent findings, Astrup and colleagues pooled data across up to 15 other studies, comparing RMR in formerly obese subjects and matched never-obese controls. Formerly obese subjects had a mean relative RMR 3-5% lower than that of control subjects (values adjusted for fat-free and fat masses; difference not statistically significant). Of the subjects with a low RMR, significantly more were formerly obese (15.3% vs 3.3%), and this could entirely account for the 3-5% lower mean.
Taken together, these results seem to indicate that a metabolic energy reduction after weight loss that exceeds simple predictions based on the reduced body weight/fat mass might occur in individuals.
So: Expect to feel hungrier and to have to stay at the same or lower calorie count and/or exercise more to maintain the weight loss.
Effects on responses to visual food stimuli
When Rosenbaum and colleagues studied 6 obese subjects in a single-blind crossover study of changes in neural activity by fMRI following a 10% weight reduction, they found decreased leptin levels and in response to visual food stimuli increased brain activity in areas related to emotional, executive, and sensory responses to food and decreased activity in areas related to emotional and cognitive control of food intake and integration of motor planning. These brain effects act to make food even more rewarding. These effects seem to be related to reduced leptin levels because administration of leptin after weight loss reversed many of these changes.
So: Expect to find food even more appealing. Manage these drives so that you're not deprived but stay at the same or lower calorie count overall.
What works to keep off the weight
The National Weight Control Registry, established in 1994, tracks over 10,000 people who have lost significant amounts of weight (at least 30 lbs) and kept it off for significant periods (at least a year). Some of the findings from registry studies are as follows:
More predictive of weight regain:
o More recent weight loss (less than 2 vs. more than 2 years)
o Larger weight loss (more than 30%)
o Dietary disinhibition (lack of restraint)
o Higher percent fat
o Negative affect (anger, anxiety)
o Adverse life events
Behavioral strategies or other factors associated with weight loss maintenance:
o Higher protein intake
o Fat intake control
o Healthy diet
o Consistent diet across weekdays and weekends
o Involvement in meal preparation
o Eating at home/fewer restaurant meals
o More frequent meals
o Eating breakfast every day
o Slower eating
o Higher levels of physical activity (especially strenuous)
o More frequent self-weighing
o Keeping records of food intake or exercise
o Keeping healthy foods in the house
o Buying health-related books or magazines
o Spending less time with overweight friends
o Continued adherence to diet and exercise strategies
o Low levels of depression and disinhibition
o Behavioral retraining to learn not to eat in response to affective and cognitive triggers
o Less TV watching (in 1 study, 62% watched ≤10 hours/week, 36% <5 hours/week)
• The risk of relapse/weight gain decreased over time. Subjects who maintained weight losses for longer periods of time reported that less effort and attention were required to diet and to maintain weight. However, these findings may be biased (individuals who find maintenance to be taxing and unpleasurable may be less likely to maintain their weight losses, and so may not be represented).
• Disinhibition due to internal cues such as feelings and thoughts triggering eating was associated with less weight loss after 6 months (significant) and 18 months (not significant), and predicted more weight regain at 1 year (significant). External disinhibition such as social events triggering eating was not significantly associated with these outcomes.
In conclusion, while homeostasis seems to be working against us, it's good to know what we're up against. The level of dogged persistence required to keep weight off seems daunting, but still, over 10,000 people have met that challenge. The main point seems to be that healthy eating and physical activity are not short-term endeavors but rather a lifelong journey. Don't even bother if you're not in for the long haul. But if we understand how our bodies respond to weight loss and are prepared for those responses, we can practice mastery, day by day, poco a poco, over our evolutionary wiring... and hopefully avoid becoming part of the dismal obesity statistics.
Blogger: Ginny Fleming, Founder, Lucidize Medical & Scientific Editing. Chief capacities: medical, scientific, and technical writing and editing.